My research in the Bonci lab is composed of two projects, one which deals with synaptic input to the VTA and one which deals with output from the VTA. The former project studies the relationship between serotonin and glutamate inputs. One question within this field is whether these two neurotransmitters are co-released from the same terminals. To address this question I am collaborating with the lab of Dr. Marisela Morales. Transgenic mice with cre recombinase expression restricted to serotonergic neurons will be used to turn on expression of virally introduced Channelrhodopsin-2 protein in serotonergic cells. Acute slices of the VTA will be cut from these mice and examined for light-induced glutamatergic currents using whole cell patch clamp techniques. A second project of mine is addressing output of the VTA. While it has been known for a long time that the VTA contains dopaminergic and non-dopaminergic projection neurons, tools have only been available to study dopaminergic neurons. This has recently changed, and with the intersection of optogenetics and mouse genetics we are now able to study these non-dopaminergic neurons. My project will use virally-delivered fluorophores and/or Channelrhodopsin-2 protein to address the following series of questions. Where do these non-dopaminergic neurons project, and are their terminal fields different from dopaminergic VTA projections? What types of currents are elicited by stimulation of these terminals, and do their synaptic properties change following exposure to drugs of abuse? Through investigation of these questions we hope to clarify the role of the VTA in drug addiction.